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      Recombinant Adenovirus siRNA Knocking Down the Ndufs4 Gene Alleviates Myocardial Apoptosis Induced by Oxidative Stress Injury

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      Author(s): 1 , 2 , 3 , 1 ,
      Publication date (Electronic):
      Journal: Cardiology Research and Practice
      Publisher: Hindawi

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          Abstract

          Oxidative stress results in myocardial cell apoptosis and even life-threatening heart failure in myocardial ischemia-reperfusion injury. Specific blocking of the complex I could reduce cell apoptosis. Ndufs4 is a nuclear-encoded subunit of the mitochondrial complex I and participates in the electron transport chain. In this study, we designed and synthesized siRNA sequences knocking down the rat Ndufs4 gene, constructed recombinant adenovirus Ndufs4 siRNA (Ad-Ndufs4 siRNA), and primarily verified the role of Ndufs4 in oxidative stress injury. The results showed that the adenovirus infection rate was about 90%, and Ndufs4 mRNA and protein were decreased by 76.7% and 64.9%, respectively. Furthermore, the flow cytometry assay indicated that the cell apoptosis rate of the Ndufs4 siRNA group was significantly decreased as compared with the H 2O 2-treated group. In conclusion, we successfully constructed Ndufs4 siRNA recombinant adenovirus; furthermore, the downexpression of the Ndufs4 gene may alleviate H 2O 2-induced H9c2 cell apoptosis.

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          Current Mechanistic Concepts in Ischemia and Reperfusion Injury.

          GIOU-TENG YIANG, Meng-Yu Wu, Andy Tsai … (2018)
          Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal dysfunction, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Ischemia-reperfusion injury is a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially the involvement of reactive oxygen species and cell death pathways. The involvement of the NADPH oxidase system, nitric oxide synthase system, and xanthine oxidase system are also described. When the blood supply is re-established after prolonged ischemia, local inflammation and ROS production increase, leading to secondary injury. Cell damage induced by prolonged ischemia-reperfusion injury may lead to apoptosis, autophagy, necrosis, and necroptosis. We highlight the latest mechanistic insights into reperfusion-injury-induced cell death via these different processes. The interlinked signaling pathways of cell death could offer new targets for therapeutic approaches. Treatment approaches for ischemia-reperfusion injury are also reviewed. We believe that understanding the pathophysiology ischemia-reperfusion injury will enable the development of novel treatment interventions.
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            Cell biology of ischemia/reperfusion injury.

            Theodore Kalogeris, Christopher P Baines, Maike Krenz … (2012)
            Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Reperfusion injury and reactive oxygen species: The evolution of a concept☆

              D. Granger, Peter R. Kvietys (2015)
              Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury. As a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain. The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.g., Nox) to activate and enhance ROS production by a second source (e.g., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.
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                Author and article information

                Contributors
                Aijun Xu:
                ORCID: https://orcid.org/0000-0003-4115-3137
                Journal
                Journal ID (nlm-ta): Cardiol Res Pract
                Journal ID (iso-abbrev): Cardiol Res Pract
                Journal ID (publisher-id): crp
                Title: Cardiology Research and Practice
                Publisher: Hindawi
                ISSN (Print): 2090-8016
                ISSN (Electronic): 2090-0597
                Publication date Collection: 2023
                Publication date (Electronic): 27 January 2023
                Volume: 2023
                Electronic Location Identifier: 8141129
                Affiliations
                1Department of Anesthesiology, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China
                2Department of Anesthesiology, Huashan Hospital of Fudan University, Shanghai, China
                3Third Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, China
                Author notes

                Academic Editor: Michael S. Wolin

                Author information
                https://orcid.org/0000-0003-4115-3137
                Article
                DOI: 10.1155/2023/8141129
                PMC ID: 9897913
                PubMed ID: 36741296
                SO-VID: 14ba530e-eb73-4086-8d0f-3708554d535d
                Copyright © Copyright © 2023 Beibei Wang et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 28 August 2022
                Date revision received : 2 December 2022
                Date accepted : 19 December 2022
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81300101
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Cardiovascular Medicine
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine

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